17β-HSD Double Nickase Plasmid (h): sc-402072-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- 17β-HSD Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- 17β-HSD Double Nickase Plasmid (h) and 17β-HSD Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HSD17B1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: 17β-HSD Antibody (D-8): sc-373902
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
17β-HSD Double Nickase Plasmid (h) | sc-402072-NIC | 20 µg | $410.00 | |||
17β-HSD Double Nickase Plasmid (h2) | sc-402072-NIC-2 | 20 µg | $410.00 |
Human HSD17B1 encodes 17β-HSD (17β-hydroxysteroid dehydrogenase type 1), a key oxidoreductase that catalyzes the conversion of estrone to the more potent estrogen estradiol and contributes to local steroid hormone homeostasis. By regulating estrogen/androgen balance, 17β-HSD integrates into steroidogenic and endocrine signaling pathways that influence transcriptional programs controlling cell proliferation, differentiation, and metabolism. Altered HSD17B1 activity or expression has been associated with hormone-dependent pathophysiology and dysregulated estrogen signaling in multiple tissues. As a result, HSD17B1 is widely studied in models of steroid metabolism, receptor-driven gene regulation, and endocrine-related disease mechanisms.
17β-HSD Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HSD17B1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HSD17B1. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt HSD17B1 function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of HSD17B1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.